|Year : 2015 | Volume
| Issue : 3 | Page : 304-307
Exploring association between sleep deprivation and chronic periodontitis: A pilot study
Vishakha Grover, Ranjan Malhotra, Harleen Kaur
Department of Periodontology and Oral Implantology, National Dental College and Hospital, Dera Bassi, Punjab, India
|Date of Submission||03-Apr-2014|
|Date of Acceptance||23-Feb-2015|
|Date of Web Publication||26-Jun-2015|
House No: 3192, Sector 37 D, Chandigarh
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Sleep deprivation has become a global phenomenon, and epidemiologic data indicate that short sleep duration adversely impacts human physical health. Underlying mechanisms involve modulation of immune-inflammatory mechanisms. These changes might contribute to potentiation of destructive periodontal disease. Therefore, the present study aimed to assess if there is an association of sleep deprivation with chronic periodontal diseases. Materials and Methods: Sixty subjects were categorized into 3 groups (n = 20 each) viz. clinically healthy, gingivitis and periodontitis. Periodontal status of subjects was assessed by gingival index and pocket probing depth. All the study subjects were administered Pittsburgh Sleep Quality Index (PSQI) questionnaire for the assessment of sleep deprivation. Results: Present investigation revealed that mean PSQI was highest in the periodontitis group as compared to other two groups and the difference among three groups was statistically significant. Conclusion: The present study with preliminary results suggestive of the association of sleep deprivation with severity of periodontal disease, definitely calls on for future studies with larger samples.
Keywords: Chronic periodontitis, Pittsburgh Sleep Quality Index, sleep deprivation
|How to cite this article:|
Grover V, Malhotra R, Kaur H. Exploring association between sleep deprivation and chronic periodontitis: A pilot study. J Indian Soc Periodontol 2015;19:304-7
|How to cite this URL:|
Grover V, Malhotra R, Kaur H. Exploring association between sleep deprivation and chronic periodontitis: A pilot study. J Indian Soc Periodontol [serial online] 2015 [cited 2021 Jun 15];19:304-7. Available from: https://www.jisponline.com/text.asp?2015/19/3/304/154173
| Introduction|| |
Periodontitis is a ubiquitous chronic inflammatory disease affecting the supporting structures of the teeth and if not promptly diagnosed and correctly managed can ultimately lead to tooth loss.  The importance of successful management and treatment of periodontitis has gained added importance in recent years with the recognition that periodontitis is associated with a number of important systemic diseases, include cardio/cerebrovascular diseases, diabetes, respiratory diseases, gastric ulcers, rheumatoid arthritis, obesity, cognitive impairment and even cancers etc.  Three basic mechanisms have been postulated to play a role in these interactions; metastatic infections, inflammation and inflammatory injury, and adaptive immunity. 
Periodontal diseases are inflammatory diseases in which microbial etiologic factors induce a series of host responses that mediate inflammatory events. In susceptible individuals, dysregulation of inflammatory and immune pathways leads to chronic inflammation, tissue destruction, and disease.  A number of risk factors contribute to the susceptibility of individuals to periodontal diseases, and to the pathogenesis and severity of the disease. These factors include smoking, diabetes, immunosuppression, genetic factors, stress, and age. Studies on how the risk factors influence disease progression have mainly been focused on the inflammatory reaction. The conclusion from these studies is that a sound inflammatory host response is needed for successful periodontal defense. Factors that modify this response may either cause an overwhelming reaction or an inadequate reaction, both of which may accelerate tissue destruction. 
The word sleep means relaxation, rest or just a light term, but it is a complex and essential biological process that is required on a daily basis for all humans regardless of age, sex or ethnic origin. In addition to maintaining normal brain functioning, sleep has important roles in controlling the functions of many other body systems vital to health and well-being.  Sleep deprivation is becoming increasingly common in today's society. Compared to a few decades ago, major changes in sleep culture have been observed globally because there has been a trend toward adopting a 24/7 lifestyle, longer working hours and longer work shifts. Medical conditions and social and domestic responsibilities further contribute to sleep restriction. This has led to a significant reduction in total sleeping hours in both adults and children.
Epidemiologic data indicate that sleep disturbance and short sleep duration adversely impact human physical health and mortality risk. ,,,,,,,, Underlying mechanisms include decrease in overall immunity, a state of systemic inflammation with increased inflammatory markers ensues, and up-regulation of hormones. ,,, Thus, in recent years, there has been an increasing body of research investigating role of sleep deprivation in pathogenesis of various chronic inflammatory and infectious diseases; however, to the best of our knowledge, the role of sleep in chronic periodontal disease has not been investigated. Therefore, the aim of the present study was to assess if there is an association of sleep deprivation with chronic periodontal diseases.
| Materials and methods|| |
A total of 60 subjects categorized in 3 groups (n = 20 each) viz. clinically healthy, gingivitis and periodontitis were identified and selected from among the patients visiting the Department of Periodontology and Oral Implantology, National Dental College and Hospital, Dera Bassi (Punjab). All study subjects underwent detailed medical history and periodontal examination before enrollment which also included information for demographics such as age, gender, and socioeconomic status. As none of the subjects belonged to poor or rich classes, subjects were categorized into low middle class, middle class, and high middle class on the basis of collected data.
Subjects were excluded if they were edentulous, pregnant or lactating, smokers, suffering from known systemic diseases which could alter healing response of periodontium, who had received any periodontal treatment in 6 months before study or those who had history of medication (antibiotics or anti-inflammatory drugs) in 3 months before study. Subjects were examined by a single examiner for the assessment of gingival index (GI) (Loe, 1963) and pocket probing depth (PPD). William's periodontal probe was used to measure the PPD from the gingival margin to the bottom of the periodontal sulcus or pocket at two proximal sites of each tooth.
The Pittsburgh Sleep Quality Index
- Group I - Healthy: GI score: 0, PPD ≤ 3 mm
- Group II - Gingivitis: GI score ≥ 1, PPD ≤ 3 mm
- Group III - Moderate to severe generalized chronic periodontitis: Generalized - PPD ≥ 3 in ≥30% of sites; moderate-severe periodontitis - PPD ≥ 6 mm
All the study subjects were administered PSQI questionnaire. The PSQI is an effective instrument used to measure the quality and patterns of sleep in the older adult. It is brief, reliable, valid, and standardized self-reported measure of sleep quality. It differentiates "poor" from "good" sleep by measuring seven domains: Subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleep medication, and daytime dysfunction over the last month. All subjects rated each of these seven areas of sleep. PSQI questionnaire was modified from the original in order to include the first 9 items only these items contribute to the total score.
Scoring of the answers was based on a 0 to 3 scale, whereby 3 reflected the negative extreme on the Likert scale. The component scores were summed to produce a global score (range 0 to 21). A global sum of "5" or greater indicated a "poor" sleeper. Higher PSQI scores represented worse sleep quality. 
All statistical analyses were carried out using Statistical Package for Social Sciences version 15.0 (SPSS Inc., Chicago, IL, USA) software package. Descriptive data were presented as mean and standard deviation. ANOVA test was used for comparison between means of groups and to determine the significance of each parameter under study. Multivariate Tukey honest significant difference test was used to investigate the relationship between global PSQI scores and other independent variables. Correlations among the variables were calculated using the Pearson's correlation coefficient. ANOVA test of between-subjects effects was used to investigate the role of confounders such as age, gender, and socioeconomic status on the relationship of PSQI and periodontal disease.
| Results|| |
Sixty systemically healthy subjects (34 females and 26 males) in age group of 25-50 years were assessed for association of sleep deprivation with chronic periodontal disease.
Present study revealed that mean GI in group I, II and III were 0, 1.39 ± 0.32 and 1.88 ± 0.18, respectively, whereas PPD were 2.08 ± 0.06, 2.34 ± 0.17 and 3.58 ± 0.63, respectively [Table 1] and [Figure 1]. Mean PSQI score in three groups was 1.20 ± 0.83, 1.88 ± 0.18, and 7.39 ± 1.33, respectively. Intergroup comparison of PSQI scores was significantly different amongst all three groups [Table 2]. The results showed a positive correlation of PSQI with GI and PPD in gingivitis and periodontitis groups [Table 3]. ANOVA test of between-subjects effects revealed that after controlling for age, gender, and socioeconomic status, association of PSQI and periodontal disease was still significant between the 3 groups, viz., healthy, gingivitis and periodontitis [Table 4].
|Table 4: Tests of between-subjects effects for analysis of the effect of age, gender, and socioeconomic status on PSQI |
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| Discussion|| |
The current investigation was aimed at assessing association of sleep deprivation with chronic periodontal disease. Results of the present investigation elucidated that mean PSQI was highest in the periodontitis group followed by gingivitis subjects and lowest in healthy subjects and the difference among three groups was statistically significant. A positive correlation of PSQI with GI and PPD was observed in groups I and II suggesting that PSQI scores commensurate with periodontal destruction. The association was still significant after controlling for age, gender, and socioeconomic status.
Varieties of methods have been utilized for assessment of sleep quantity and quality like administration of the questionnaire, clinical interviews, sleep diaries, etc., In our study, we have selected PSQI for assessing sleep deprivation. The PSQI has 89.6% sensitivity and 86.5% specificity for identifying "good" and "bad" sleep using a cut-off global score of 5.It also has internal consistency and a reliability coefficient (Cronbach's alpha) of 0.83 for its seven components. Numerous studies using the PSQI in a variety of older adult population internationally have supported high validity and reliability. 
The study findings could not be subjected to direct comparison with any with any earlier similar investigation because to best of our knowledge this is a first investigation conducted for exploring association of sleep deprivation with periodontal disease. But essentially there exists biological plausibility for such findings. Sleep deprivation leads to the development of unfavorable hormonal profile and modulation of host immune and inflammatory mechanisms. Deprivation of sleep has been documented to increase lymphocyte activation with overproductions of interleukin-1 (IL-1), IL-6, IL-17, and tumor necrosis factor alpha (TNF-α). , An important start in the efforts to find the source of sleep loss-associated inflammation is a work showing that one night of sleep restricted to 4 h led to increased monocyte production of IL-6 and TNF-alpha messenger RNA. , During experimental sleep deprivation of healthy volunteers, cellular adhesion molecules have been found to increase which are pro-coagulatory and pro-inflammatory markers produced by stimulated vascular endothelium (e.g. E-selectin and intercellular adhesion molecule-1). ,
Sleep-wake cycles have also emerged as prominent regulators of the immune system. Central nervous system regulation of immune responses is primarily driven by two effector signaling pathways: Activation of the hypothalamic pituitary adrenal (HPA) axis and the sympathetic nervous system (SNS). Sleep loss activates sympathetic activity with less robust evidence of effects on the HPA axis. Whereas activation of HPA axis inhibits both antiviral and pro-inflammatory genes, SNS activation suppresses antiviral responses (Th1-type gene expression such as interferon-g and IL-12B) while stimulating pro-inflammatory genes (Th2-type cytokine genes such as IL-4 and IL-5), which together provides a plausible mechanism to connect sleep disturbance with various infectious and inflammatory diseases. Thus, sleep deprivation decreases immunity and ensues systemic inflammation. , As many of cytokines have a significant role in the pathogenesis of chronic periodontal disease, there might occur potentiation of periodontal destruction in a sleep deprived individual. Further short sleep duration has been shown not only to increase pathogen susceptibility; but also to decrease the immunologic protection offered by standard vaccines. ,,,
Sleep deprivation is known to adversely affect cognition and motor performance.  This might impair an individual's capacity to perform adequate oral hygiene practices, thus increasing the risk of periodontal disease. Due to multifactorial etiology of both sleep deprivation and periodontal disease other unknown confounding factors might explain this association too.
Thus, the present study can be taken as hypothesis generating investigation and with its preliminary results suggestive of the association of sleep deprivation with severity of periodontal disease, definitely calls on for future studies with larger samples, studying the effects after controlling of other confounding factors and including both subjective and objective measures for assessment of sleep.
| Conclusion|| |
Within limits of the present investigation, there appears to be an association between periodontal diseases and sleep deprivation. Better understanding the interplay between sleep deprivation and periodontitis with more focused investigations may help in designing effective lifestyle intervention strategies for this multifactorial disease.
| References|| |
Nowjack-Raymer RE, Sheiham A. Association of edentulism and diet and nutrition in US adults. J Dent Res 2003;82:123-6.
Linden GJ, Lyons A, Scannapieco FA. Periodontal systemic associations: Review of the evidence. J Periodontol 2013;84:S8-19.
Van Dyke TE, van Winkelhoff AJ. Infection and inflammatory mechanisms. J Periodontol 2013;84:S1-7.
Cekici A, Kantarci A, Hasturk H, Van Dyke TE. Inflammatory and immune pathways in the pathogenesis of periodontal disease. Periodontol 2000 2014;64:57-80.
Pöllänen MT, Salonen JI, Uitto VJ. Structure and function of the tooth-epithelial interface in health and disease. Periodontol 2000 2003;31:12-31.
Aldabal L, Bahammam AS. Metabolic, endocrine, and immune consequences of sleep deprivation. Open Respir Med J 2011;5:31-43.
Cohen S, Doyle WJ, Alper CM, Janicki-Deverts D, Turner RB. Sleep habits and susceptibility to the common cold. Arch Intern Med 2009;169:62-7.
Dew MA, Hoch CC, Buysse DJ, Monk TH, Begley AE, Houck PR, et al.
Healthy older adults' sleep predicts all-cause mortality at 4 to 19 years of follow-up. Psychosom Med 2003;65:63-73.
Dørheim SK, Bondevik GT, Eberhard-Gran M, Bjorvatn B. Sleep and depression in postpartum women: A population-based study. Sleep 2009;32:847-55.
Irwin MR. Sleep and infectious disease risk. Sleep 2012;35:1025-6.
Wolk R, Gami AS, Garcia-Touchard A, Somers VK. Sleep and cardiovascular disease. Curr Probl Cardiol 2005;30:625-62.
Ogawa Y, Kanbayashi T, Saito Y, Takahashi Y, Kitajima T, Takahashi K, et al.
Total sleep deprivation elevates blood pressure through arterial baroreflex resetting: A study with microneurographic technique. Sleep 2003;26:986-9.
Patel SR, Malhotra A, Gao X, Hu FB, Neuman MI, Fawzi WW. A prospective study of sleep duration and pneumonia risk in women. Sleep 2012;35:97-101.
Singh M, Drake CL, Roehrs T, Hudgel DW, Roth T. The association between obesity and short sleep duration: A population-based study. J Clin Sleep Med 2005;1:357-63.
Mullington JM, Simpson NS, Meier-Ewert HK, Haack M. Sleep loss and inflammation. Best Pract Res Clin Endocrinol Metab 2010;24:775-84.
Irwin MR, Cole SW. Reciprocal regulation of the neural and innate immune systems. Nat Rev Immunol 2011;11:625-32.
Irwin M, Thompson J, Miller C, Gillin JC, Ziegler M. Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: Clinical implications. J Clin Endocrinol Metab 1999;84:1979-85.
Irwin MR, Wang M, Campomayor CO, Collado-Hidalgo A, Cole S. Sleep deprivation and activation of morning levels of cellular and genomic markers of inflammation. Arch Intern Med 2006;166:1756-62.
Frey DJ, Fleshner M, Wright KP Jr. The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults. Brain Behav Immun 2007;21:1050-7.
Buysse DJ, Reynolds CF 3 rd
, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh Sleep Quality Index: A new instrument for psychiatric practice and research. Psychiatry Res 1989;28:193-213.
Sauvet F, Leftheriotis G, Gomez-Merino D, Langrume C, Drogou C, Van Beers P, et al.
Effect of acute sleep deprivation on vascular function in healthy subjects. J Appl Physiol (1985) 2010;108:68-75.
Lange T, Dimitrov S, Bollinger T, Diekelmann S, Born J. Sleep after vaccination boosts immunological memory. J Immunol 2011;187:283-90.
Lange T, Perras B, Fehm HL, Born J. Sleep enhances the human antibody response to hepatitis A vaccination. Psychosom Med 2003;65:831-5.
Prather AA, Hall M, Fury JM, Ross DC, Muldoon MF, Cohen S, et al.
Sleep and antibody response to hepatitis B vaccination. Sleep 2012;35:1063-9.
Spiegel K, Sheridan JF, Van Cauter E. Effect of sleep deprivation on response to immunization. JAMA 2002;288:1471-2.
Durmer JS, Dinges DF. Neurocognitive consequences of sleep deprivation. Semin Neurol 2005;25:117-29.
[Table 1], [Table 2], [Table 3], [Table 4]